Interleukin-1 alpha mediates an alternative pathway for the antiproliferative action of poly(I.C) on human endothelial cells.

Garfinkel, Susan; Haines, Dale S.; Brown, Sondi; Wessendorf, J; Gillespie, David; Maciag, Thomas

doi:10.1016/s0021-9258(18)35776-4

Cited by 30 publications

(5 citation statements)

References 35 publications

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“…Total RNA was isolated by the guanidinium isothyocyanate procedure as previously described (24). The RNA was electrophoresed on an 0.8% (wt/ vol) agarose gel containing 2.2 M formaldehyde, capillary-blotted onto nylon membrane filters (Zeta-Probe; Bio-Rad Laboratories), and hybridized to 32 P-labeled DNA probes at 65 Њ C for 20 h. Filters were washed at high stringency and exposed to Kodak XAR films (Eastman Kodak Co., Rochester, NY).…”

Section: Rna Extraction and Analysismentioning

confidence: 99%

Activation of the MAP Kinase Pathway by FGF-1 Correlates with Cell Proliferation Induction While Activation of the Src Pathway Correlates with Migration

LaVallee

Prudovsky

McMahon

et al. 1998

The Journal of Cell Biology

121

101

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FGF regulates both cell migration and proliferation by receptor-dependent induction of immediate-early gene expression and tyrosine phosphorylation of intracellular polypeptides. Because little is known about the disparate nature of intracellular signaling pathways, which are able to discriminate between cell migration and proliferation, we used a washout strategy to examine the relationship between immediate-early gene expression and tyrosine phosphorylation with respect to the potential of cells either to migrate or to initiate DNA synthesis in response to FGF-1. We demonstrate that transient exposure to FGF-1 results in a significant decrease in Fos transcript expression and a decrease in tyrosine phosphorylation of the FGFR-1, p42mapk, and p44mapk. Consistent with these biochemical effects, we demonstrate that attenuation in the level of DNA synthesis such that a 1.5-h withdrawal is sufficient to return the population to a state similar to quiescence. In contrast, the level of Myc mRNA, the activity of Src, the tyrosine phosphorylation of cortactin, and the FGF-1–induced redistribution of cortactin and F-actin were unaffected by transient FGF-1 stimulation. These biochemical responses are consistent with an implied uncompromised migratory potential of the cells in response to growth factor withdrawal. These results suggest a correlation between Fos expression and the mitogen-activated protein kinase pathway with initiation of DNA synthesis and a correlation between high levels of Myc mRNA and Src kinase activity with the regulation of cell migration.

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Section: Rna Extraction and Analysismentioning

confidence: 99%

Activation of the MAP Kinase Pathway by FGF-1 Correlates with Cell Proliferation Induction While Activation of the Src Pathway Correlates with Migration

LaVallee

Prudovsky

McMahon

et al. 1998

The Journal of Cell Biology

121

101

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“…Total RNA was extracted from HUVEC monolayers by the guanidinium isothiocyanate procedure as described (14). RNA (10 I~g) was separated on 0.8% agarose gels and capillary-blotted onto Zeta-Probe nylon membranes (BioRad Labs, Hercules, CA).…”

Section: Rna Extraction Northern Blot Analysis and Reverse Transcriptase-polymerase Chain Reactionmentioning

confidence: 99%

“…Reverse transcription polymerase chain reaction (RT-PCR) was performed using 1 I~g total RNA as described (14). The eDNA was diluted with 1-t20 to 500 txl and PCR was performed with 5 I~1 of each sample amplified by denaturation at 94°C for 1 min, annealed at 54°C for 2 rain, and elongated at 72°C for 3 min using 35 cycles for the FGFR family and 32 cycles for GAPDH.…”

Section: Rna Extraction Northern Blot Analysis and Reverse Transcriptase-polymerase Chain Reactionmentioning

confidence: 99%

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FGF-1-dependent proliferative and migratory responses are impaired in senescent human umbilical vein endothelial cells and correlate with the inability to signal tyrosine phosphorylation of fibroblast growth factor receptor-1 substrates.

Garfinkel

Prudovsky

et al. 1996

The Journal of Cell Biology

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Abstract. Senescent cells do not proliferate in response to exogenous growth factors, yet the number and affinity of growth factor receptors on the cell surface appear to be similar to presenescent cell populations. To determine whether a defect in receptor signaling exists, we analyzed human umbilical vein endothelial cells (HU-VEC) since HUVEC growth is absolutely dependent upon the presence of FGF. We report that in both presenescent and senescent HUVEC populations, FGF-1 induces the expression of cell cycle-specific genes, suggesting that functional FGF receptor (FGFR) may exist on the surface of these cells. However, the tyrosine phosphorylation of FGFR-1 substrates, Src and cortactin, is impaired in senescent HUVEC, and only the presenescent cell populations exhibit a FGF-l-dependent Src tyrosine kinase activity. Moreover, we demonstrate that senescent HUVEC are unable to migrate in response to FGF-1, and these data correlate with an altered organization of focal adhesion sites. These data suggest that the induction of gene expression is insufficient to promote a proliferative or migratory phenotype in senescent HUVEC and that the attenuation of the FGFR-1 signal transduction pathway may be involved in the inability of senescent HUVEC to proliferate and/or migrate.

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“…Ultimately, the specific effect exerted by these factors on cell homeostasis may depend on the different timing, context and levels of IL-1α expression, integrating with other locally acting cytokines. It was indeed demonstrated that endogenous IL-1 α can bidirectionally regulate cell growth (Cozzolino et al 1990, Garfinkel et al 1992, an effect that can be mediated by IL-1α -modulated Cdks/Cdk inhibitors, as recently shown (Zeki et al 1999). The tightly controlled expression of cellexpressed IL-1α which thus appears essential for homeostasis of privileged organs, can be assured by controlling either IL-1 α generation and secretion or/and its cytosolic activity via modification of structure (i.e.…”

Section: Low Expression Of Il-1 In Privileged Organsmentioning

confidence: 99%

Distinct Patterns of IL-L&#X03B1; and IL-L&#X03B2; Organ Distribution-A Possible Basis for Organ Mechanisms of Innate Immunity

Hacham

Argov

White

et al. 2002

Advances in Experimental Medicine and Biology

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Interleukin-1 alpha mediates an alternative pathway for the antiproliferative action of poly(I.C) on human endothelial cells.

Cited by 30 publications

References 35 publications

Activation of the MAP Kinase Pathway by FGF-1 Correlates with Cell Proliferation Induction While Activation of the Src Pathway Correlates with Migration

Activation of the MAP Kinase Pathway by FGF-1 Correlates with Cell Proliferation Induction While Activation of the Src Pathway Correlates with Migration

FGF-1-dependent proliferative and migratory responses are impaired in senescent human umbilical vein endothelial cells and correlate with the inability to signal tyrosine phosphorylation of fibroblast growth factor receptor-1 substrates.

Distinct Patterns of IL-L&#X03B1; and IL-L&#X03B2; Organ Distribution-A Possible Basis for Organ Mechanisms of Innate Immunity

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